Influence of Dietary Zinc, Copper and Cadmium Levels on Rat Liver Aryl Sulfotransferase Ⅳ Activity|RISS 상세보기

다국어 초록 (Multilingual Abstract)

Aryl sulfotransferase (AST) Ⅳ is a liver enzyme involved in detoxication and has been shown to be susceptible to down regulation by a number of hepatotoxic xenobiotics. Studies presented here to investigate the ability of biological and non-biological divalent metal cations on AST Ⅳ activity showed that AST Ⅳ was strongly inhibited following in vitro or in vivo exposure to. Zn (Ⅱ), Co (Ⅱ) or Cd (Ⅱ). It was found that 0.025~2.5 ㎛ of these metal ions were sufficient to cause 50% of inhibition in vitro in purified AST Ⅳ and 0.25~25 ㎛ of these metal ions in liver cytosolic fractions. For the in vivo study, 1,000 ㎎ Cu (Ⅱ)/㎏, 2,000 ㎎ Zn (Ⅱ)/㎏ or 250 ㎎ Cd (Ⅱ)/㎏ was added to individual diets and administered to three (3) groups of rats over a 7 week period The Cu (Ⅱ)-supplemented diet produced no apparent change in rat growth rote and resulted in 30-fold increase in liver cytotolic Cu (Ⅱ) levels, suggesting that elevated levels of Cu (Ⅱ) ion in the liver were responsible for the loss of AST Ⅳ activity. In contrast, the Zn (Ⅱ)-supplemented diet caused a decrease in rot growth rates and resulted in zero increase in liver Zn (Ⅱ) levels, which suggested an indirect inhibition mechanism was caused by Zn (Ⅱ) in the liver. Rats were fed the Cd-supplemented diet also displayed a decrease in growth rote with little or no change in liver Cu (Ⅱ) or Zn (Ⅱ) levels. When the liver cytosols of rots from the metal ion diets were immunochemically analyzed for the AST Ⅳ and albumin contents, no significant changes were observed in albumin levels. However, AST Ⅳ contents in the cytosols of mts fed the Zn (Ⅱ)-supplemented diets showed a slight decrease in amount. These results showed that AST Ⅳ activity in vitro and in vivo can be inhibited by Cu (Ⅱ), Zn (Ⅱ), and Cd (Ⅱ) by apparently different mechanisms. The immediate response to a Zn injection showed a decrease in AST Ⅳ activity but not in the AST Ⅳ content in liver cytosol. These mechanisms appeared to involve direct actions of the metal ion on AST Ⅳ activity and indirect actions affecting AST Ⅳ amount.

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목차 (Table of Contents)

INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
Literature Cited

INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
Literature Cited

참고문헌 (Reference)

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